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Microbial ligand costimulation drives neutrophilic steroid-refractory asthma

(2015) PLOS ONE. 10(8).
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Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
Abstract
Asthma is a heterogeneous disease whose etiology is poorly understood but is likely to involve innate responses to inhaled microbial components that are found in allergens. The influence of these components on pulmonary inflammation has been largely studied in the context of individual agonists, despite knowledge that they can have synergistic effects when used in combination. Here we have explored the effects of LPS and beta-glucan, two commonly-encountered microbial agonists, on the pathogenesis of allergic and non-allergic respiratory responses to house dust mite allergen. Notably, sensitization with these microbial components in combination acted synergistically to promote robust neutrophilic inflammation, which involved both Dectin-1 and TLR-4. This pulmonary neutrophilic inflammation was corticosteroid-refractory, resembling that found in patients with severe asthma. Thus our results provide key new insights into how microbial components influence the development of respiratory pathology.
Keywords
DISEASE, INHALED ANTIGEN, RECEPTOR DECTIN-1, IMMUNE-RESPONSE, HOUSE-DUST MITE, ALLERGIC AIRWAY INFLAMMATION, BETA-GLUCANS, INNATE IMMUNITY, CLADOSPORIUM-CLADOSPORIOIDES, DENDRITIC CELLS

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Citation

Please use this url to cite or link to this publication:

Chicago
Hadebe, Sabelo, Frank Kirstein, Kaat Fierens, Kong Chen, Rebecca A Drummond, Simon Vautier, Sara Sajaniemi, et al. 2015. “Microbial Ligand Costimulation Drives Neutrophilic Steroid-refractory Asthma.” Plos One 10 (8).
APA
Hadebe, S., Kirstein, F., Fierens, K., Chen, K., Drummond, R. A., Vautier, S., Sajaniemi, S., et al. (2015). Microbial ligand costimulation drives neutrophilic steroid-refractory asthma. PLOS ONE, 10(8).
Vancouver
1.
Hadebe S, Kirstein F, Fierens K, Chen K, Drummond RA, Vautier S, et al. Microbial ligand costimulation drives neutrophilic steroid-refractory asthma. PLOS ONE. 2015;10(8).
MLA
Hadebe, Sabelo et al. “Microbial Ligand Costimulation Drives Neutrophilic Steroid-refractory Asthma.” PLOS ONE 10.8 (2015): n. pag. Print.
@article{6971803,
  abstract     = {Asthma is a heterogeneous disease whose etiology is poorly understood but is likely to involve innate responses to inhaled microbial components that are found in allergens. The influence of these components on pulmonary inflammation has been largely studied in the context of individual agonists, despite knowledge that they can have synergistic effects when used in combination. Here we have explored the effects of LPS and beta-glucan, two commonly-encountered microbial agonists, on the pathogenesis of allergic and non-allergic respiratory responses to house dust mite allergen. Notably, sensitization with these microbial components in combination acted synergistically to promote robust neutrophilic inflammation, which involved both Dectin-1 and TLR-4. This pulmonary neutrophilic inflammation was corticosteroid-refractory, resembling that found in patients with severe asthma. Thus our results provide key new insights into how microbial components influence the development of respiratory pathology.},
  articleno    = {e0134219},
  author       = {Hadebe, Sabelo and Kirstein, Frank and Fierens, Kaat and Chen, Kong and Drummond, Rebecca A and Vautier, Simon and Sajaniemi, Sara and Murray, Graeme and Williams, David L and Redelinghuys, Pierre and Reinhart, Todd A and Junecko, Beth A Fallert and Kolls, Jay K and Lambrecht, Bart and Brombacher, Frank and Brown, Gordon D},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keywords     = {DISEASE,INHALED ANTIGEN,RECEPTOR DECTIN-1,IMMUNE-RESPONSE,HOUSE-DUST MITE,ALLERGIC AIRWAY INFLAMMATION,BETA-GLUCANS,INNATE IMMUNITY,CLADOSPORIUM-CLADOSPORIOIDES,DENDRITIC CELLS},
  language     = {eng},
  number       = {8},
  pages        = {17},
  title        = {Microbial ligand costimulation drives neutrophilic steroid-refractory asthma},
  url          = {http://dx.doi.org/10.1371/journal.pone.0134219},
  volume       = {10},
  year         = {2015},
}

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